Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Discovery of a druggable copper-signaling pathway that drives inflammation

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus Homo sapiens

PROVIDER: GSE160864 | GEO | 2023/03/03

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Discovery of a druggable copper-signaling pathway that drives inflammation

Project description:Quantitative mass-spectrometry-based proteomics in MDM during inflammation.

2023-04-06 | PXD038612 | Pride

A druggable copper-signalling pathway that drives inflammation.

Project description:Inflammation is a complex physiological process triggered in response to harmful stimuli1. It involves cells of the immune system capable of clearing sources of injury and damaged tissues. Excessive inflammation can occur as a result of infection and is a hallmark of several diseases2-4. The molecular bases underlying inflammatory responses are not fully understood. Here we show that the cell surface glycoprotein CD44, which marks the acquisition of distinct cell phenotypes in the context of development, immunity and cancer progression, mediates the uptake of metals including copper. We identify a pool of chemically reactive copper(II) in mitochondria of inflammatory macrophages that catalyses NAD(H) redox cycling by activating hydrogen peroxide. Maintenance of NAD+ enables metabolic and epigenetic programming towards the inflammatory state. Targeting mitochondrial copper(II) with supformin (LCC-12), a rationally designed dimer of metformin, induces a reduction of the NAD(H) pool, leading to metabolic and epigenetic states that oppose macrophage activation. LCC-12 interferes with cell plasticity in other settings and reduces inflammation in mouse models of bacterial and viral infections. Our work highlights the central role of copper as a regulator of cell plasticity and unveils a therapeutic strategy based on metabolic reprogramming and the control of epigenetic cell states.

| S-EPMC10131557 | biostudies-literature

Discovery of a druggable copper-signaling pathway that drives inflammation

Project description:Discovery of a druggable copper-signaling pathway that drives inflammation

| PRJNA674654 | ENA

Endothelial TGFb signaling drives vascular inflammation and atherosclerosis

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-08-26 | GSE134558 | GEO

Targeting Myc signaling pathway by inhibition of histone demethylase JMJD2B

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-01-01 | E-GEOD-45970 | biostudies-arrayexpress

JNK1 Signaling Downstream of the EGFR Pathway Contributes to Imiquimod-induced Skin Inflammation

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-01-12 | GSE164581 | GEO

An ectopic network of transcription factors regulated by Hippo signaling drives growth and invasion of a malignant tumor model

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-06-10 | E-GEOD-71354 | biostudies-arrayexpress

PDGF Engages an E2F-USP1 Signaling Pathway to Support ID2-mediated Survival of Proneural Glioma Cells.

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-03-22 | E-GEOD-77424 | biostudies-arrayexpress

cGAS/STING drives ageing-related inflammation and neurodegeneration

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-08-20 | GSE234422 | GEO

Chronic inflammation decreases HSC fitness by activating the druggable Jak/Stat3 signaling pathway.

Project description:Chronic inflammation represents a major threat to human health since long-term systemic inflammation is known to affect distinct tissues and organs. Recently, solid evidence demonstrated that chronic inflammation affects hematopoiesis; however, how chronic inflammation affects hematopoietic stem cells (HSCs) on the mechanistic level is poorly understood. Here, we employ a mouse model of chronic multifocal osteomyelitis (CMO) to assess the effects of a spontaneously developed inflammatory condition on HSCs. We demonstrate that hematopoietic and nonhematopoietic compartments in CMO BM contribute to HSC expansion and impair their function. Remarkably, our results suggest that the typical features of murine multifocal osteomyelitis and the HSC phenotype are mechanistically decoupled. We show that the CMO environment imprints a myeloid gene signature and imposes a pro-inflammatory profile on HSCs. We identify IL-6 and the Jak/Stat3 signaling pathway as critical mediators. However, while IL-6 and Stat3 blockage reduce HSC numbers in CMO mice, only inhibition of Stat3 activity significantly rescues their fitness. Our data emphasize the detrimental effects of chronic inflammation on stem cell function, opening new venues for treatment.

| S-EPMC9827550 | biostudies-literature

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data